Loading…

miR-25 Promotes Cell Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Targeting the LATS2/YAP Signaling Pathway

Metastasis is the leading cause of high mortality in lung cancer patients, and metastatic lung cancer is difficult to treat. miRNAs are involved in various biological processes of cancer, including metastasis. Our previous studies revealed that miR-25 promoted non-small-cell lung cancer (NSCLC) cell...

Full description

Saved in:
Bibliographic Details
Published in:Oxidative medicine and cellular longevity 2019, Vol.2019 (2019), p.1-14
Main Authors: Ning, Yong, Li, Yong, Lu, Zhongxin, Yan, Ge, Zheng, Chao, Liu, Shuiyi, Li, Xiaoyi, Jiang, Liyuan, Zhang, Tianzhu, Hu, Hui, Wu, Tangwei, Chen, Weiqun
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c499t-a6a0c3911004f188eb248edd42c18ab55297c66c983ec753d84a11b050c0dc823
cites cdi_FETCH-LOGICAL-c499t-a6a0c3911004f188eb248edd42c18ab55297c66c983ec753d84a11b050c0dc823
container_end_page 14
container_issue 2019
container_start_page 1
container_title Oxidative medicine and cellular longevity
container_volume 2019
creator Ning, Yong
Li, Yong
Lu, Zhongxin
Yan, Ge
Zheng, Chao
Liu, Shuiyi
Li, Xiaoyi
Jiang, Liyuan
Zhang, Tianzhu
Hu, Hui
Wu, Tangwei
Chen, Weiqun
description Metastasis is the leading cause of high mortality in lung cancer patients, and metastatic lung cancer is difficult to treat. miRNAs are involved in various biological processes of cancer, including metastasis. Our previous studies revealed that miR-25 promoted non-small-cell lung cancer (NSCLC) cell proliferation and suppressed cell apoptosis by directly targeting TP53 and MOAP1. In this work, we further explored the miR-25 expression in NSCLC patients in the Cancer Genome Atlas (TCGA) database and measured the miR-25 expression levels in the tissues of NSCLC patients and cell lines. miR-25 was overexpressed in both NSCLC tissues and cell lines. NSCLC patients who expressed a higher level of miR-25 exhibited worse overall survival than those with a lower level of miR-25. Overexpression of miR-25 enhanced NSCLC cell migration and invasion, while the inhibition of miR-25 exhibited the opposite effects. We identified the large tumor suppressor homology 2 (LATS2) as a new target gene of miR-25 in lung cancer. The effects of miR-25 on promoting NSCLC cell migration and invasion were at least partially due to activation of the Hippo signaling pathway. Additionally, miR-25 antagomir inhibited xenograft tumor growth and metastasis by the upregulation of LATS2. Taken together, our findings demonstrate that miR-25 contribute to lung cancer cell proliferation and metastasis by targeting the LATS2/YAP signaling pathway, which implicate miR-25 as a promising therapeutic target for lung cancer metastasis. Given that oxidative stress induces the overexpression of miR-25 and plays a critical role in cancer progression, this study establishes miR-25 as an intermediate between oxidative stress and lung cancer metastasis.
doi_str_mv 10.1155/2019/9719723
format article
fullrecord <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6604298</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A603153388</galeid><sourcerecordid>A603153388</sourcerecordid><originalsourceid>FETCH-LOGICAL-c499t-a6a0c3911004f188eb248edd42c18ab55297c66c983ec753d84a11b050c0dc823</originalsourceid><addsrcrecordid>eNqNks9v0zAUxyMEYlvhxhlZ4oLEQv0jTuLLpKpiMKlARcuBk_XqOKmnxB52sqn_AH83ztp1wImT33v--Pv8tV-SvCL4PSGcTykmYioKIgrKniSnRGQ0xUJkT48xxifJWQjXGOeMZuR5csIII3nkT5NfnfmWUo6W3nWu1wHNdduOWWtq7aE3zp6jz6Z5CMFW6MreQogZcjX64my66qBt0_uDi8E2aA5WaY82O7QG3-jexFq_1WgxW6_o9MdsiVamsdCO9SX02zvYvUie1dAG_fKwTpLvlx_W80_p4uvHq_lskapMiD6FHLBighCMs5qUpd7QrNRVlVFFSthwTkWh8lyJkmlVcFaVGRCywRwrXKmSsklysde9GTadrpS2vYdW3njTgd9JB0b-vWPNVjbuVuY5zmiUnSRvDwLe_Rx06GVngorWwWo3BEkpFwIXvMgi-uYf9NoNPvq-pzBnXOTskWqg1dLY2sW-ahSVsxwzwhkrx7bne0p5F4LX9fHKBMtxDOQ4BvIwBhF__afNI_zw7xF4twe2xlZwZ_5TTkdG1_BIUzw-DPsNoiXBqw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2250535963</pqid></control><display><type>article</type><title>miR-25 Promotes Cell Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Targeting the LATS2/YAP Signaling Pathway</title><source>Wiley Online Library website</source><source>Publicly Available Content (ProQuest)</source><creator>Ning, Yong ; Li, Yong ; Lu, Zhongxin ; Yan, Ge ; Zheng, Chao ; Liu, Shuiyi ; Li, Xiaoyi ; Jiang, Liyuan ; Zhang, Tianzhu ; Hu, Hui ; Wu, Tangwei ; Chen, Weiqun</creator><contributor>Moorthy, Bhagavatula ; Bhagavatula Moorthy</contributor><creatorcontrib>Ning, Yong ; Li, Yong ; Lu, Zhongxin ; Yan, Ge ; Zheng, Chao ; Liu, Shuiyi ; Li, Xiaoyi ; Jiang, Liyuan ; Zhang, Tianzhu ; Hu, Hui ; Wu, Tangwei ; Chen, Weiqun ; Moorthy, Bhagavatula ; Bhagavatula Moorthy</creatorcontrib><description>Metastasis is the leading cause of high mortality in lung cancer patients, and metastatic lung cancer is difficult to treat. miRNAs are involved in various biological processes of cancer, including metastasis. Our previous studies revealed that miR-25 promoted non-small-cell lung cancer (NSCLC) cell proliferation and suppressed cell apoptosis by directly targeting TP53 and MOAP1. In this work, we further explored the miR-25 expression in NSCLC patients in the Cancer Genome Atlas (TCGA) database and measured the miR-25 expression levels in the tissues of NSCLC patients and cell lines. miR-25 was overexpressed in both NSCLC tissues and cell lines. NSCLC patients who expressed a higher level of miR-25 exhibited worse overall survival than those with a lower level of miR-25. Overexpression of miR-25 enhanced NSCLC cell migration and invasion, while the inhibition of miR-25 exhibited the opposite effects. We identified the large tumor suppressor homology 2 (LATS2) as a new target gene of miR-25 in lung cancer. The effects of miR-25 on promoting NSCLC cell migration and invasion were at least partially due to activation of the Hippo signaling pathway. Additionally, miR-25 antagomir inhibited xenograft tumor growth and metastasis by the upregulation of LATS2. Taken together, our findings demonstrate that miR-25 contribute to lung cancer cell proliferation and metastasis by targeting the LATS2/YAP signaling pathway, which implicate miR-25 as a promising therapeutic target for lung cancer metastasis. Given that oxidative stress induces the overexpression of miR-25 and plays a critical role in cancer progression, this study establishes miR-25 as an intermediate between oxidative stress and lung cancer metastasis.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2019/9719723</identifier><identifier>PMID: 31316723</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; Apoptosis ; Biomarkers ; Cancer ; Cancer therapies ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - genetics ; Cell Proliferation - physiology ; China ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Genomes ; Health aspects ; Humans ; Kinases ; Lung cancer ; Lung cancer, Non-small cell ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Medical prognosis ; Metastasis ; MicroRNA ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Mortality ; Oxidative stress ; Pathogenesis ; Prostate ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; Signal Transduction ; Survival analysis ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Tumor proteins ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism</subject><ispartof>Oxidative medicine and cellular longevity, 2019, Vol.2019 (2019), p.1-14</ispartof><rights>Copyright © 2019 Tangwei Wu et al.</rights><rights>COPYRIGHT 2019 John Wiley &amp; Sons, Inc.</rights><rights>Copyright © 2019 Tangwei Wu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Tangwei Wu et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-a6a0c3911004f188eb248edd42c18ab55297c66c983ec753d84a11b050c0dc823</citedby><cites>FETCH-LOGICAL-c499t-a6a0c3911004f188eb248edd42c18ab55297c66c983ec753d84a11b050c0dc823</cites><orcidid>0000-0001-8838-1714 ; 0000-0002-4628-2117 ; 0000-0002-3365-0881</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2250535963/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2250535963?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,4024,25753,27923,27924,27925,37012,37013,44590,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31316723$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Moorthy, Bhagavatula</contributor><contributor>Bhagavatula Moorthy</contributor><creatorcontrib>Ning, Yong</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><creatorcontrib>Lu, Zhongxin</creatorcontrib><creatorcontrib>Yan, Ge</creatorcontrib><creatorcontrib>Zheng, Chao</creatorcontrib><creatorcontrib>Liu, Shuiyi</creatorcontrib><creatorcontrib>Li, Xiaoyi</creatorcontrib><creatorcontrib>Jiang, Liyuan</creatorcontrib><creatorcontrib>Zhang, Tianzhu</creatorcontrib><creatorcontrib>Hu, Hui</creatorcontrib><creatorcontrib>Wu, Tangwei</creatorcontrib><creatorcontrib>Chen, Weiqun</creatorcontrib><title>miR-25 Promotes Cell Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Targeting the LATS2/YAP Signaling Pathway</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Metastasis is the leading cause of high mortality in lung cancer patients, and metastatic lung cancer is difficult to treat. miRNAs are involved in various biological processes of cancer, including metastasis. Our previous studies revealed that miR-25 promoted non-small-cell lung cancer (NSCLC) cell proliferation and suppressed cell apoptosis by directly targeting TP53 and MOAP1. In this work, we further explored the miR-25 expression in NSCLC patients in the Cancer Genome Atlas (TCGA) database and measured the miR-25 expression levels in the tissues of NSCLC patients and cell lines. miR-25 was overexpressed in both NSCLC tissues and cell lines. NSCLC patients who expressed a higher level of miR-25 exhibited worse overall survival than those with a lower level of miR-25. Overexpression of miR-25 enhanced NSCLC cell migration and invasion, while the inhibition of miR-25 exhibited the opposite effects. We identified the large tumor suppressor homology 2 (LATS2) as a new target gene of miR-25 in lung cancer. The effects of miR-25 on promoting NSCLC cell migration and invasion were at least partially due to activation of the Hippo signaling pathway. Additionally, miR-25 antagomir inhibited xenograft tumor growth and metastasis by the upregulation of LATS2. Taken together, our findings demonstrate that miR-25 contribute to lung cancer cell proliferation and metastasis by targeting the LATS2/YAP signaling pathway, which implicate miR-25 as a promising therapeutic target for lung cancer metastasis. Given that oxidative stress induces the overexpression of miR-25 and plays a critical role in cancer progression, this study establishes miR-25 as an intermediate between oxidative stress and lung cancer metastasis.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Apoptosis</subject><subject>Biomarkers</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Proliferation - physiology</subject><subject>China</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung cancer, Non-small cell</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Mortality</subject><subject>Oxidative stress</subject><subject>Pathogenesis</subject><subject>Prostate</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Signal Transduction</subject><subject>Survival analysis</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor proteins</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNqNks9v0zAUxyMEYlvhxhlZ4oLEQv0jTuLLpKpiMKlARcuBk_XqOKmnxB52sqn_AH83ztp1wImT33v--Pv8tV-SvCL4PSGcTykmYioKIgrKniSnRGQ0xUJkT48xxifJWQjXGOeMZuR5csIII3nkT5NfnfmWUo6W3nWu1wHNdduOWWtq7aE3zp6jz6Z5CMFW6MreQogZcjX64my66qBt0_uDi8E2aA5WaY82O7QG3-jexFq_1WgxW6_o9MdsiVamsdCO9SX02zvYvUie1dAG_fKwTpLvlx_W80_p4uvHq_lskapMiD6FHLBighCMs5qUpd7QrNRVlVFFSthwTkWh8lyJkmlVcFaVGRCywRwrXKmSsklysde9GTadrpS2vYdW3njTgd9JB0b-vWPNVjbuVuY5zmiUnSRvDwLe_Rx06GVngorWwWo3BEkpFwIXvMgi-uYf9NoNPvq-pzBnXOTskWqg1dLY2sW-ahSVsxwzwhkrx7bne0p5F4LX9fHKBMtxDOQ4BvIwBhF__afNI_zw7xF4twe2xlZwZ_5TTkdG1_BIUzw-DPsNoiXBqw</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Ning, Yong</creator><creator>Li, Yong</creator><creator>Lu, Zhongxin</creator><creator>Yan, Ge</creator><creator>Zheng, Chao</creator><creator>Liu, Shuiyi</creator><creator>Li, Xiaoyi</creator><creator>Jiang, Liyuan</creator><creator>Zhang, Tianzhu</creator><creator>Hu, Hui</creator><creator>Wu, Tangwei</creator><creator>Chen, Weiqun</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley &amp; Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8838-1714</orcidid><orcidid>https://orcid.org/0000-0002-4628-2117</orcidid><orcidid>https://orcid.org/0000-0002-3365-0881</orcidid></search><sort><creationdate>2019</creationdate><title>miR-25 Promotes Cell Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Targeting the LATS2/YAP Signaling Pathway</title><author>Ning, Yong ; Li, Yong ; Lu, Zhongxin ; Yan, Ge ; Zheng, Chao ; Liu, Shuiyi ; Li, Xiaoyi ; Jiang, Liyuan ; Zhang, Tianzhu ; Hu, Hui ; Wu, Tangwei ; Chen, Weiqun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-a6a0c3911004f188eb248edd42c18ab55297c66c983ec753d84a11b050c0dc823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Apoptosis</topic><topic>Biomarkers</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Proliferation - physiology</topic><topic>China</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lung cancer, Non-small cell</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Mortality</topic><topic>Oxidative stress</topic><topic>Pathogenesis</topic><topic>Prostate</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Signal Transduction</topic><topic>Survival analysis</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Tumor proteins</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumor Suppressor Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ning, Yong</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><creatorcontrib>Lu, Zhongxin</creatorcontrib><creatorcontrib>Yan, Ge</creatorcontrib><creatorcontrib>Zheng, Chao</creatorcontrib><creatorcontrib>Liu, Shuiyi</creatorcontrib><creatorcontrib>Li, Xiaoyi</creatorcontrib><creatorcontrib>Jiang, Liyuan</creatorcontrib><creatorcontrib>Zhang, Tianzhu</creatorcontrib><creatorcontrib>Hu, Hui</creatorcontrib><creatorcontrib>Wu, Tangwei</creatorcontrib><creatorcontrib>Chen, Weiqun</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health &amp; Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest research library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content (ProQuest)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ning, Yong</au><au>Li, Yong</au><au>Lu, Zhongxin</au><au>Yan, Ge</au><au>Zheng, Chao</au><au>Liu, Shuiyi</au><au>Li, Xiaoyi</au><au>Jiang, Liyuan</au><au>Zhang, Tianzhu</au><au>Hu, Hui</au><au>Wu, Tangwei</au><au>Chen, Weiqun</au><au>Moorthy, Bhagavatula</au><au>Bhagavatula Moorthy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-25 Promotes Cell Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Targeting the LATS2/YAP Signaling Pathway</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2019</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>14</epage><pages>1-14</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Metastasis is the leading cause of high mortality in lung cancer patients, and metastatic lung cancer is difficult to treat. miRNAs are involved in various biological processes of cancer, including metastasis. Our previous studies revealed that miR-25 promoted non-small-cell lung cancer (NSCLC) cell proliferation and suppressed cell apoptosis by directly targeting TP53 and MOAP1. In this work, we further explored the miR-25 expression in NSCLC patients in the Cancer Genome Atlas (TCGA) database and measured the miR-25 expression levels in the tissues of NSCLC patients and cell lines. miR-25 was overexpressed in both NSCLC tissues and cell lines. NSCLC patients who expressed a higher level of miR-25 exhibited worse overall survival than those with a lower level of miR-25. Overexpression of miR-25 enhanced NSCLC cell migration and invasion, while the inhibition of miR-25 exhibited the opposite effects. We identified the large tumor suppressor homology 2 (LATS2) as a new target gene of miR-25 in lung cancer. The effects of miR-25 on promoting NSCLC cell migration and invasion were at least partially due to activation of the Hippo signaling pathway. Additionally, miR-25 antagomir inhibited xenograft tumor growth and metastasis by the upregulation of LATS2. Taken together, our findings demonstrate that miR-25 contribute to lung cancer cell proliferation and metastasis by targeting the LATS2/YAP signaling pathway, which implicate miR-25 as a promising therapeutic target for lung cancer metastasis. Given that oxidative stress induces the overexpression of miR-25 and plays a critical role in cancer progression, this study establishes miR-25 as an intermediate between oxidative stress and lung cancer metastasis.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>31316723</pmid><doi>10.1155/2019/9719723</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-8838-1714</orcidid><orcidid>https://orcid.org/0000-0002-4628-2117</orcidid><orcidid>https://orcid.org/0000-0002-3365-0881</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1942-0900
ispartof Oxidative medicine and cellular longevity, 2019, Vol.2019 (2019), p.1-14
issn 1942-0900
1942-0994
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6604298
source Wiley Online Library website; Publicly Available Content (ProQuest)
subjects Adaptor Proteins, Signal Transducing - genetics
Adaptor Proteins, Signal Transducing - metabolism
Apoptosis
Biomarkers
Cancer
Cancer therapies
Carcinoma, Non-Small-Cell Lung - genetics
Carcinoma, Non-Small-Cell Lung - metabolism
Carcinoma, Non-Small-Cell Lung - pathology
Cell cycle
Cell growth
Cell Line, Tumor
Cell Proliferation - genetics
Cell Proliferation - physiology
China
Gene expression
Gene Expression Regulation, Neoplastic
Genetic aspects
Genomes
Health aspects
Humans
Kinases
Lung cancer
Lung cancer, Non-small cell
Lung Neoplasms - genetics
Lung Neoplasms - metabolism
Lung Neoplasms - pathology
Medical prognosis
Metastasis
MicroRNA
MicroRNAs - genetics
MicroRNAs - metabolism
Mortality
Oxidative stress
Pathogenesis
Prostate
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
Signal Transduction
Survival analysis
Transcription Factors - genetics
Transcription Factors - metabolism
Tumor proteins
Tumor Suppressor Proteins - genetics
Tumor Suppressor Proteins - metabolism
title miR-25 Promotes Cell Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Targeting the LATS2/YAP Signaling Pathway
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T18%3A13%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=miR-25%20Promotes%20Cell%20Proliferation,%20Migration,%20and%20Invasion%20of%20Non-Small-Cell%20Lung%20Cancer%20by%20Targeting%20the%20LATS2/YAP%20Signaling%20Pathway&rft.jtitle=Oxidative%20medicine%20and%20cellular%20longevity&rft.au=Ning,%20Yong&rft.date=2019&rft.volume=2019&rft.issue=2019&rft.spage=1&rft.epage=14&rft.pages=1-14&rft.issn=1942-0900&rft.eissn=1942-0994&rft_id=info:doi/10.1155/2019/9719723&rft_dat=%3Cgale_pubme%3EA603153388%3C/gale_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c499t-a6a0c3911004f188eb248edd42c18ab55297c66c983ec753d84a11b050c0dc823%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2250535963&rft_id=info:pmid/31316723&rft_galeid=A603153388&rfr_iscdi=true